The purpose of this research program is to understand vascular adaptation within skeletal muscle in response to acute and chronic exposure to exercise. We have shown that exercise training produces an increase in the capacity of skeletal muscle vascular beds to transport nutrients to the muscle. The data suggest that this increase is most evident in the muscle tissue with the greatest relative increase in activity during the training bouts. The experiments will test the hypothesis that training induced angiogenesis occurs specifically in and around the muscle fibers that are required to have the largest increase in activity during the training bouts and that intense endurance training results in increased endurance to prolonged exercise due to these changes in the skeletal muscle vasculature combined with increases in maximal cardiac output. We will also test the hypothesis that these adaptations occur in all mammals by determining if similar vascular adaptations are seen in trained miniature swine. Finally, the study of the mechanisms responsible for skeletal muscle exercise hyperemia will be continued. Experiments will be conducted to determine the role of the "muscle pump" mechanism in muscle perfusion during exercise. Skeletal muscle vascular function will continue to be assessed with measurements of total and regional blood flows, capillary permeability surface-area products, capillary filtration coefficients, capillary protein osmotic reflection coefficients, isogravimetric capillary pressures, total resistance, pre- and post-capillary resistances and standard hemodynamics. Whole body oxygen consumption, arterial and venous blood gases and lactates will be measured in miniature swine during exercise and biochemical, anatomical and morphometric indexes of training induced adaptations in skeletal muscle will also be obtained to elucidate the interactions of exercise, oxygen transport systems, and skeletal muscle biochemistry. These studies will reveal adaptive mechanisms involved in and among oxygen transport systems (central and peripheral) and skeletal muscle oxidative biochemical pathways in response to acute and chronic increases in metabolic demand.